Ligaments are load-bearing structures that connect two skeletal members. Tendons are load-bearing structures that attach muscle to bone. Occasionally, the natural ligament and tendon will fail or need repair. The generally accepted method of reconstruction of ligaments and tendons is through the use of tissue transplanted to the defect site from elsewhere in the body. Reconstructions often fail due to a number of factors, including insufficient strength of the transplanted tissues, dependence of the transplanted tissue on revascularization for viability and inadequate strength of attachment or fixation of the transplanted tissue.
There have also been many attempts to develop a prosthetic replacement for damaged ligaments and tendons. Many of these attempts have often either failed or have brought on a new set of complications.
It is generally recognized that one of the necessary properties for a successful ligament or tendon prosthesis is ultimate fixation by host tissue. This is desirable because fixation by screws, staples, or other rigid devices is unlikely to persist without deterioration of fixation strength over time. Many attempts have been made to provide for tissue ingrowth into a prosthetic ligament device. Included among these attempts are:
(1) U.S. Pat. Nos. 3,971,670; 4,127,902; and 4,129,470 to Homsy; U.S. Pat. No. 4,149,277 to Bokros and 4,668,233 to Seedhom et al, all of which teach attachment through tissue ingrowth into porous areas of the prosthetic devices;
2) U.S. Pat. No. 3,613,120 to MacFarland; U.S. Pat. No. 3,545,008 to Bader; and U.S. Pat. Nos. 4,209,859 and 4,483,023 to Hoffman; all of which teach tissue attachment to porous fabrics with various methods of maintaining apposition to the repaired tissue.
An expanded polytetrafluoroethylene prosthetic ligament, described in U.S. Pat. No. 5,049,155 teaches the use of expanded polytetrafluoroethylene (hereinafter PTFE) in a single continuous filament looped to form parallel strands in which the strands are fixed together at the ends to form at least one eyelet. This product has proved to be a significant improvement over the above devices. In some circumstances, however, there has been evidence of non-uniform tensile loading across the cross-section of the prosthesis arising from non-uniform fixation by tissue and of stress concentrations and abrasion in areas where there is contact with bone edges.
In prosthetic devices that allow for tissue ingrowth, the ingrowth by host tissues may be a non-uniform occurrence whereby sections of the prosthetic device may become well fixed by tissue attachment while others may not become fixed at all. Non-uniformity is especially apparent during the period when tissue begins to grow into the device. The net effect of this variable tissue fixation is a great variation in the effective length of load-bearing members. As tissue grows into some portions of the prosthesis, the effective lengths of those portions are shortened to the distance between where the ingrowth has occurred. This is illustrated in FIG. 1a wherein the length of non-ingrown load-bearing members is the distance between the two fixation sites as designated by L.sub.0 and the shortened length of ingrown load-bearing members is designated by L.sub.1. When the prosthesis is subjected to tensile loading, those shorter load-bearing members which are fixed by tissue undergo a greater strain than those members which have no ingrowth. Consequently, the shorter members are subject to rupture first. Upon the rupture of these members, the loads are transferred to the next shortest members, and so on, causing a progressive rupture of the cross-section of the prosthesis at a relatively low load.
Another failure mode of prosthetic ligaments or tendons is a result of the methods of attachment to bony skeletal members. Many of these methods involve drilling tunnels in the connecting bones, routing the prosthesis through the tunnels, and fixing the ends to the bones. In vivo, prosthetic devices are subject to tension and flexion at multiple sites along the longitudinal axis of the device causing high stress concentrations at these sites. These stress concentrations, combined with relative movement of the prosthesis, may result in early failures due to abrasion and multi-site rupture of individual load-bearing members. Two major sites of impingement of a cruciate ligament prosthesis in the knee, for example, are the intra-articular bone tunnel exits on the tibia and femur, with various other sites in the intercondylar notch of the femur as well.
The severity of multiple site damage to a multistranded prosthesis is due to the accumulation of damage. This is illustrated in FIG. 1b wherein a hypothetical prosthesis has a total of 6 load-bearing members. In FIG. 1b, three strands are cut at one site and three strands are cut at another site. The prosthesis has lost all of its tensile strength since there are no intact load-bearing members left. This example illustrates how even slight to moderate damage at several different sites can result in severe or total loss of strength of the prosthesis due to the cumulative effect of local damage.